哮喘-COPD重叠综合征的病理生理学解释：轻度小叶中心型肺气肿可引起从不吸烟、长期呼吸气流受限的哮喘患者的肺弹性回缩力下
2015/07/16
摘要
研究者认为，尽管存在气道重塑和气道高反应性，大多数哮喘患者通过治疗可逆转气流阻塞。有吸烟和非吸烟患者在接受治疗后仍存在COPD，并同时具有哮喘和COPD的特征。研究者将这类难治患者称为哮喘-COPD重叠综合征（ACOS）。另外，一部分接受过治疗的、不吸烟的中度至重度哮喘患者存在持续性呼吸气流限制，尽管部分可逆。这被认为由大气道，尤其是小气道重塑所导致。另一方面，我们及其他研究者描述了不吸烟的中重度慢性哮喘患者中可逆的急性和长期肺弹性回缩力下降及其对最大呼吸量的不良影响。由于缺乏结构-功能方面的研究，符合ACOS的非吸烟慢性哮喘患者中肺弹性回缩力下降及长期呼吸气流阻塞的机制尚未知。我们近期报导了一起对10例不吸烟的、接受过治疗的、存在长期呼吸气流阻塞（部分可逆）的哮喘患者的病理生理学观察（Gelb AF et al. Letters to Editor. JACI 2014; 133: 263-5）。所有10名哮喘患者肺弹性回缩力均显著下降，并在所有的3例尸检中意外发现显微镜下轻度小叶中心型肺气肿，肺部CT不易发现此情况。这些前哨的病理生理学观察结果需要进一步的证实以阐明ACOS的附带现象。导致肺部组织分解的促炎症反应和蛋白溶解机制需要进一步的研究。
（苏欣 审校）
Chest. 2015 May 7. doi: 10.1378/chest.14-2483. [Epub ahead of print]
Unraveling the Pathophysiology of the Asthma COPD Overlap Syndrome: Unsuspected mild centrilobular emphysema is responsible for loss of lung elastic recoil in never smoked asthmatics with persistent expiratory airflow limitation.
Gelb AF, Yamamoto A, Verbeken EK, Nadel JA.
Abstract
Investigators believe most asthmatics have reversible airflow obstruction with treatment, despite airway remodeling and hyperresponsiveness. There are smoking and non-smoking patients with chronic expiratory airflow obstruction despite treatment, who have features of both asthma and chronic obstructive pulmonary disease. Investigators refer to this conundrum as the Asthma COPD Overlap Syndrome (ACOS). Furthermore, a subset of treated, non-smoking moderate-to-severe asthmatics, have persistent expiratory airflow limitation, despite partial reversibility. It has been assumed to be due to large and especially small airway remodeling. Alternatively, we and others have described reversible loss of lung elastic recoil in acute and persistent loss in moderate-to-severe chronic asthmatics who never smoked, and its adverse effect on maximal expiratory airflow. The mechanism(s) responsible for loss of lung elastic recoil and persistent expiratory airflow limitation in chronic non-smoking asthmatics consistent with ACOS remain unknown in the absence of structure-function studies. We recently reported a new pathophysiologic observation in 10 never-smoked, treated asthmatics with persistent expiratory airflow obstruction, despite partial reversibility (Gelb AF et al. Letters to Editor. JACI 2014; 133: 263-5). All 10 asthmatics had a significant decrease in lung elastic recoil, and unsuspected, microscopic mild centrilobular emphysema was noted in all 3 autopsies obtained, but was not easily identified on lung CT. These sentinel pathophysiologic observations need to be confirmed to further unravel the epiphenomenon of ACOS. The proinflammatory and proteolytic mechanism(s) leading to lung tissue breakdown need to be further investigated.
Chest. 2015 May 7. doi: 10.1378/chest.14-2483. [Epub ahead of print]
